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Antithrombin–Heparin Complexes
Published in Severian Dumitriu, Valentin Popa, Polymeric Biomaterials, 2020
Leslie R. Berry, Anthony K.C. Chan
There are only three general approaches to permanent linkage of antithrombin and heparin. Bonding can occur if heparin is activated to make it reactive, followed by interaction with antithrombin to effect covalent bond formation. Conversely, antithrombin can be pre-activated and then incubated with heparin to obtain a stable complex. Finally, antithrombin and heparin can be conjugated by allowing the two macromolecules to interact non-covalently, followed by addition of a bifunctional reagent, one end of which bonds to the serpin and the other end of which reacts covalently with the GAG. The three synthetic schemes for ATH preparation are outlined in Figure 1.4. In the first two methodologies, it is theoretically possible that the heparin or antithrombin may possess groups that, under the appropriate conditions, are already reactive enough to form a bond with the other macromolecule. Furthermore, in a number of procedures, care must be taken (either by selective chemistry, appropriate reagent stoichiometries, or particular reaction conditions) to prevent linkage of either heparin to itself or antithrombin to itself.
Fucoidan
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Ellya Sinurat, Dina Fransiska, Nurhayati, Hari Eko Irianto
Heparin is a polysaccharide that is highly sulfated and widely used in anticoagulant therapy. It has been used to demonstrate the ability of sulfated polysaccharides to interfere with biological systems. Fucoidan has shown great anticoagulant action and huge therapeutic development potential. It can prevent the activity of coagulation factors in the coagulation pathways by interacting with antithrombin (Jung et al., 2007).
Computational modeling of hypercoagulability in COVID-19
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Ge Zhu, Susree Modepalli, Mohan Anand, He Li
Accumulating evidence suggests that COVID-19 patients are prone to experience a hypercoagulable state as evident from the perturbation in the level of different coagulation factors, such as increased levels of factor V, factor VIII, factor X, fibrinogen and decreased amounts of antithrombin and protein C (Singhania et al. (2020)). Some of the abnormal factors reported in the literature are summarized in Table 1. Multiple studies based on thromboelastography (TEG), a conventional approach to measure the dynamics of clot growth, stabilization and dissolution, have demonstrated that these abnormal levels of factors are associated with the prothrombotic conditions in COVID-19 (Mortus et al. (2020); Panigada et al. (2020); Yuriditsky et al. (2020)). Clinical data has shown that COVID-19 associated coagulopathy could lead to major thrombotic complications, i.e., venous thromboembolism is a major complication of COVID-19 (Avruscio et al. (2020)). To better understand how the varied concentrations of these coagulation factors in COVID-19 increase the risk of excessive thrombus formation, we need to quantitatively simulate these concentration changes in the coagulation cascade induced by these abnormal concentration levels. Thus, the present work aims to apply two different mathematical models of human coagulation to recent COVID-19 laboratory data to study and identify potential changes in coagulation cascade dynamics, thereby providing insight for identifying potential therapeutic targets for future treatments.
Immobilizing argatroban and mPEG-NH2 on a polyethersulfone membrane surface to prepare an effective nonthrombogenic biointerface
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Yanling Dai, Siyuan Dai, Xiaohui Xie, Jianping Ning
Heparin has been extensively researched as a coating of biomaterial surfaces to inhibit thrombosis [3, 8, 18, 21, 22]. HeprAN, the membrane of the commercial Evodial dialyzer, uses improved AN69ST technology in which heparin is grafted to the membrane. Several studies show that the Evodial dialyzer can be used without the systemic administration of heparin for hemodialysis in patients with bleeding tendencies [23–27]. Although the HeprAN membrane has been proven to be non-inferior to saline infusion, the superiority of its treatment, has not been demonstrated [23, 28, 29]. Additionally, the anticoagulation effectiveness of heparin is dependent upon the patient plasma concentration of antithrombin (AT). Therefore, heparin cannot be used in patients with an AT deficiency and can only indirectly inhibit free plasma thrombin but cannot inhibit fibrin-bound thrombin [30–31]. Moreover, nonspecific binding to other molecules [32], including plasma proteins and platelet factor 4 (PF4), not only reduces the availability of heparin to bind AT but can also induce side effects [31, 33], such as heparin-induced thrombocytopenia (HIT, an adverse immune-mediated drug reaction by an anti-heparin/PF4 complex antibody), which may further increase the risk of bleeding in patients with hemorrhage complications.
Preparation of sulfonated silk fibroin for anti-coagulation material
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Jianrong Wu, Yuancong Zhao, Jin Wang, Tianxue You, Nan Huang
APTT of the 300 μg SSF is so much longer than that of the 10 μg SSF in Figure 13. This result explains that the SSF APTT has dose-dependent characteristic. After the 0.5 mg SSF was added into 1.0 ml PPP, this sample was incubated, and APTT value was examined about 160s. When the SSF concentration reached 1.67 mg/ml in PPP, the sample showed the anticoagulant effect by auto ACL 200 coagulation analyzer. So the SSF has the excellent anticoagulant function by adding 1.67 mg in 1.0 ml PPP, but the SF contrast sample has no better anticoagulant effect. APTT results reveal that the anti-coagulation property of the SSF is superior to those of the SF. This result can effectively explain that the sulfonic acid groups truly possess the anticoagulant function in the SSF molecules. The excellent improvement of the SSF hemocompatibility is achieved by introducing the sulfonic acid group into the SF molecular chain. The SSF increases the activity of antithrombin III, and inhibits the transformation of fibrinogen into fibrin. So the anticoagulant property of the SSF is enhanced on APTT, which shows the distinguished property of intrinsic anti-coagulation. The anticoagulant activity of the SSF is better than that of the SF, so it is a potential candidate for blood-contact materials.